Quiescence is a reversible state of cell cycle arrest adopted by resident stem cells of healthy tissues. Stem cells have been reported in a wide range of tissues, and reside in specialised microenvironments, termed niches. In a healthy tissue, their inactive state is advantageous as it protects from DNA damage during replication, and preserves the integrity of stem cells. Not only can these cells reawaken if appropriately stimulated, but they can continue down a differentiation lineage to restore and regenerate tissues as needed. However, quiescence has been reported in a range of cancer stem cells. Their lack of proliferation allows them to evade current therapies, such as chemotherapy and radiotherapy. We propose that quiescent stem cells display increased or diverse cell surface protein expression, potentially to facilitate communication with their specialised niche. If quiescent cancer stem cells indeed conserve this, then it is a potentially actionable therapeutic vulnerability for which drugs can be repurposed and novel therapies invented. We analysed scRNA-seq data from three healthy mouse tissues, namely neural stem cells from the hippocampus, haematopoietic stem cells from bone marrow and muscle stem cells from the muscle to determine if quiescent stem cells displayed an increase in gene expression for cell surface proteins. Following this, we analysed patient-derived snRNA-seq data, and finally performed cell surface pulldowns to examine if our initial findings were conserved at the protein level in cancer. We found that quiescent stem cells display an enrichment of cell surface protein-encoding genes regardless of tissue type and in a species-independent manner. We further validated that this is conserved proteomically. In our project, we have shown that the upregulation of cell surface genes is a conserved phenomenon in quiescent stem cells. Furthermore, we have shown that quiescent cancer stem cells conserve this in-vitro at the protein level.